Evidence map›Paper›PMID 25304854›Full record

ArticleJournal of the American Heart Association2014

Interferon regulatory factor 7 protects against vascular smooth muscle cell proliferation and neointima formation.

Ling Huang, Shu-Min Zhang, Peng Zhang, Xiao-Jing Zhang, Li-Hua Zhu, Ke Chen, Lu Gao, Yan Zhang, Xiang-Jie Kong, Song Tian and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. RNA modifications and cancer ferroptosis.Cancer cell international · 2026
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  6. ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  7. Article
  8. Review
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  10. Molecular therapy. Nucleic acids · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Ling HuangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Shu-Min ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Peng ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Xiao-Jing ZhangState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China (X.J.Z.).
Li-Hua ZhuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Ke ChenCollege of Life Sciences, Wuhan University, Wuhan, China (K.C., X.D.Z.).
Lu GaoDepartment of Cardiology, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (L.G.).
Yan ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Xiang-Jie KongDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Song TianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Xiao-Dong ZhangCollege of Life Sciences, Wuhan University, Wuhan, China (K.C., X.D.Z.).
Hongliang LiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.) Cardiovascular Research Institute of Wuhan University, Wuhan, China (L.H., S.M.Z., P.Z., L.H.Z., Y.Z., X.J.K., S.T., H.L.).
Wuhan University · CNRenmin Hospital of Wuhan University · CNUnion Hospital · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterferon regulatory factor 7 (IRF7), a member of the interferon regulatory factor family, plays important roles in innate immunity and immune cell differentiation. However, the role of IRF7 in neointima formation is currently unknown. METHODS AND

resultsSignificant decreases in IRF7 expression were observed in vascular smooth muscle cells (VSMCs) following carotid artery injury in vivo and platelet-derived growth factor-BB (PDGF-BB) stimulation in vitro. Compared with non-transgenic (NTG) controls, SMC-specific IRF7 transgenic (IRF7-TG) mice displayed reduced neointima formation and VSMC proliferation in response to carotid injury, whereas a global knockout of IRF7 (IRF7-KO) resulted in the opposite effect. Notably, a novel IRF7-KO rat strain was successfully generated and used to further confirm the effects of IRF7 deletion on the acceleration of intimal hyperplasia based on a balloon injury-induced vascular lesion model. Mechanistically, IRF7's inhibition of carotid thickening and the expression of VSMC proliferation markers was dependent on the interaction of IRF7 with activating transcription factor 3 (ATF3) and its downstream target, proliferating cell nuclear antigen (PCNA). The evidence that IRF7/ATF3-double-TG (DTG) and IRF7/ATF3-double-KO (DKO) mice abolished the regulatory effects exhibited by the IRF7-TG and IRF7-KO mice, respectively, validated the underlying molecular events of IRF7-ATF3 interaction.

conclusionsThese findings demonstrated that IRF7 modulated VSMC proliferation and neointima formation by interacting with ATF3, thereby inhibiting the ATF3-mediated induction of PCNA transcription. The results of this study indicate that IRF7 is a novel modulator of neointima formation and VSMC proliferation and may represent a promising target for vascular disease therapy.

Indexed as

Activating Transcription Factor 3AnimalsBlotting, WesternCarotid Artery InjuriesCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationInterferon Regulatory Factor-7MaleMiceMice, Inbred C57BLMice, TransgenicMicroscopy, ConfocalMuscle, Smooth, VascularMyocytes, Smooth MuscleActivating Transcription Factor 3Atf3 protein, ratInterferon Regulatory Factor-7ATF3IRF7neointima formationproliferation

Identifiers

PMID25304854
PMCPMC4323813
OpenAlexW2135133647

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.